Besides genetic predisposition towards the disorder, individuals with bulimia nervosa have also been found to have unusual levels of serotonin, norepinephrine, and dopamine (Festissov et al., 2000). Experiments performed with laboratory rats showed that when serotonin was released into either the ventromedial or lateral hypothalamus, eating stopped and the animal starved (Festissov et al., 2000).
Both the ventromedial and lateral hypothalamus have been shown to govern eating behavior in humans, as well as in many laboratory animals (Festissov et al., 2000). The ventromedial hypothalamus functions as the satiety center. When this part of the brain is stimulated, eating stops, and this feeling correlates to a feeling of being full. On the other hand, when the lateral hypothalamus is stimulated, it causes a feeling correlated with hunger and eating behavior. When functioning appropriately, these two areas work to keep the body at a particular body weight, which is known as the set point in a negative feedback loop. When either of these hypothalamic regions are damaged, a person will experience unnatural eating behaviors that reflect a new set point (Festissov et al.,